The present disclosure relates generally to valves and associated systems and methods for use in ophthalmic treatments. In some instances, embodiments of the present disclosure are configured to be part of an IOP control system.
Glaucoma, a group of eye diseases affecting the retina and optic nerve, is one of the leading causes of blindness worldwide. Most forms of glaucoma result when the intraocular pressure (IOP) increases to pressures above normal for prolonged periods of time. IOP can increase due to high resistance to the drainage of the aqueous humor relative to its production. Left untreated, an elevated IOP causes irreversible damage to the optic nerve and retinal fibers resulting in a progressive, permanent loss of vision.
The eye's ciliary body continuously produces aqueous humor, the clear fluid that fills the anterior segment of the eye (the space between the cornea and lens). The aqueous humor flows out of the anterior chamber (the space between the cornea and iris) through the trabecular meshwork and the uveoscleral pathways, both of which contribute to the aqueous drainage system. The delicate balance between the production and drainage of aqueous humor determines the eye's IOP.
FIG. 1 is a diagram of the front portion of an eye that helps to explain the processes of glaucoma. In FIG. 1, representations of the lens 110, cornea 120, iris 130, ciliary body 140, trabecular meshwork 150, and Schlemm's canal 160 are pictured. Anatomically, the anterior segment of the eye includes the structures that cause elevated IOP which may lead to glaucoma. Aqueous fluid is produced by the ciliary body 140 that lies beneath the iris 130 and adjacent to the lens 110 in the anterior segment of the eye. This aqueous humor washes over the lens 110 and iris 130 and flows to the drainage system located in the angle of the anterior chamber. The angle of the anterior chamber, which extends circumferentially around the eye, contains structures that allow the aqueous humor to drain. The trabecular meshwork 150 is commonly implicated in glaucoma. The trabecular meshwork 150 extends circumferentially around the anterior chamber. The trabecular meshwork 150 seems to act as a filter, limiting the outflow of aqueous humor and providing a back pressure that directly relates to IOP. Schlemm's canal 160 is located beyond the trabecular meshwork 150. Schlemm's canal 160 is fluidically coupled to collector channels (not shown) allowing aqueous humor to flow out of the anterior chamber. The two arrows in the anterior segment of FIG. 1 show the flow of aqueous humor from the ciliary bodies 140, over the lens 110, over the iris 130, through the trabecular meshwork 150, and into Schlemm's canal 160 and its collector channels.
One method of treating glaucoma includes implanting a drainage device in a patient's eye. The drainage device allows fluid to flow from the interior chamber of the eye to a drainage site, relieving pressure in the eye and thus lowering IOP. These devices are generally passive devices and do not provide a smart, interactive control of the amount of flow through the drainage tube. In addition, fluid filled blebs frequently develop at the drainage site. The development of the bleb typically includes fibrosis, which leads to increased flow resistance and it is generally the case that this resistance increases overtime. This development and progression of fibrosis reduces or eliminates flow from the anterior chamber, eliminating the capacity of the drainage device to affect IOP.
In an ideal scenario, bleb sizes are limited and bleb fluid is gradually absorbed into the body at a rate that matches or exceeds the drainage rate, thereby keeping the bleb size small. However, when drainage flow rates exceed the rate of absorption into the body, the bleb size and pressure may increase. Too much pressure can cause a bleb to migrate to an undesirable location or can lead to fibrosis. Fibrosis may include generation of at least some scar tissue, reducing the ability of the eye to reabsorb fluid in the location of the bleb. As the bleb continues to grow, the risk of leakage may increase, along with the effects of fibrosis. Fibrosis may also cause an increase in resistance at the drainage site of the implant and/or cause the lumens of passive implants to clog over time, causing the IOP to rise.
Furthermore, as bleb sizes increase, and the body, due to fibrosis or other conditions, cannot reabsorb the bleb fluid, bleb pressure may match the interior chamber eye pressure, reducing or eliminating flow from the interior chamber, and thereby eliminating the capacity of the drainage device to affect IOP pressure. Therefore, the performance of these passive drainage implants is often dictated by the patient's fibrotic response to the implant.
Accordingly, there exists a need for an IOP control system or implant that protects against under-filtration while simultaneously guarding against over-filtration, and consequently reduces or eliminates bleb formation and fibrotic changes. The system and methods disclosed herein overcome one or more of the deficiencies of the prior art.